Experimental autoimmune uveoretinitis (EAU) is a T-cell-mediated autoimmune disease that serves as a model of human intra-ocular inflammatory diseases (uveitis). It is initiated in susceptible animals by immunization with retinal antigens such as interphotoreceptor retinoid- binding protein (IRBP) or S-antigen (S-Ag) or by adoptive transfer of activated S-Ag- or IRBP-specific uveitogenic T lymphocytes. We had previously demonstrated that Vbeta8-expressing T cells accumulate in the retina during EAU. In FY 1993-1994, we sought to define the T-cell subsets and cytokines present in the retina of athymic and euthymic Lewis rats after adoptive transfer of uveitogenic or nonuveitogenic T lymphocytes. Our results indicate that (1) the temporal appearance of cytokine- producing T cells in the retina is influenced by the immunological status of the rat and might affect parameters such as vascular permeability that influence the penetration of lymphocytes into the eye. (2) Cytokine messenger ribonucleic acid (mRNA) transcripts were detected in the retinas of animals immunized with uveitogenic T lymphocytes, as well as in the retinas of rats injected with Con A-specific T cells. However, rats injected with Con A-specific T cells neither developed EAU nor was there detection of Vbeta8+ T cells in their retinas. (3) Detection of interferon (IFN)-gamma transcripts was temporally correlated with the appearance of Vbeta8+ T cells in the retina and the onset of disease. Taken together, our data suggest that infiltration of the retina by activated T-cells is not sufficient for disease induction; ocular-antigen specific Th1-like Vbeta8+ lymphocytes appear to be necessary for EAU induction.